ArticlePloS one2019
Pharmacological activation of the nuclear receptor REV-ERB reverses cognitive deficits and reduces amyloid-β burden in a mouse model of Alzheimer's disease.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Circadian disruption as a driver and target in neurodegenerative diseases: from molecular mechanisms to chronotherapeutic strategies.Metabolic brain disease · 2026Review
- REV-ERBs as regulators of circadian rhythm, neuroinflammation, and glial lipid homeostasis in Alzheimer's disease. A narrative review.British journal of biomedical science · 2026Review
- Core Circadian Protein BMAL1: Implication for Nervous System Functioning and Its Diseases.Brain sciences · 2025Review
- Chronic Exercise Protects Against Cognitive Deficits in an Alzheimer's Disease Model by Enhancing Autophagy and Reducing Mitochondrial Abnormalities.Molecular neurobiology · 2025Article
- REV-ERBα regulates brain NADNature aging · 2025Article
- Targeting Circadian Protein Rev-erbα to Alleviate Inflammation, Oxidative Stress, and Enhance Functional Recovery Following Brain Trauma.Antioxidants (Basel, Switzerland) · 2024Article
- Targeting the circadian modulation: novel therapeutic approaches in the management of ASD.Frontiers in psychiatry · 2024Review
- The circadian neutrophil, inside-out.Journal of leukocyte biology · 2023Review
- Rev-erbα agonist SR9009 protects against cerebral ischemic injury through mechanisms involving Nrf2 pathway.Frontiers in pharmacology · 2023Article
- Sinapic Acid Ameliorates REV-ERB α Modulated Mitochondrial Fission against MPTP-Induced Parkinson's Disease Model.Biomolecules & therapeutics · 2022Article
- The role of REV-ERB in NASH.Acta pharmacologica Sinica · 2022Article
- Targeting whole body metabolism and mitochondrial bioenergetics in the drug development for Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022Review
- A Growing Link between Circadian Rhythms, Type 2 Diabetes Mellitus and Alzheimer's Disease.International journal of molecular sciences · 2022Review
- A Dichotomous Role for FABP7 in Sleep and Alzheimer's Disease Pathogenesis: A Hypothesis.Frontiers in neuroscience · 2022Article
- Effects of the Clock Modulator Nobiletin on Circadian Rhythms and Pathophysiology in Female Mice of an Alzheimer's Disease Model.Biomolecules · 2021Article
- Melatonin inhibits RANKL‑induced osteoclastogenesis through the miR‑882/Rev‑erbα axis in Raw264.7 cells.International journal of molecular medicine · 2021Article
- The Molecular Clock and Neurodegenerative Disease: A Stressful Time.Frontiers in molecular biosciences · 2021Review
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Alzheimer's disease currently lacks treatment options that effectively reverse the biological/anatomical pathology and cognitive deficits associated with the disease. Loss of function of the nuclear receptor REV-ERB is associated with reduced cognitive function in mouse models. The effect of enhanced REV-ERB activity on cognitive function has not been examined. In this study, we tested the hypothesis that enhanced REV-ERB function may enhance cognitive function in a model of Alzheimer's disease. We utilized the REV-ERB agonist SR9009 to pharmacologically activate the activity of REV-ERB in the SAMP8 mouse model of Alzheimer's disease. SR9009 reversed cognitive dysfunction of an aged SAMP8 mouse in several behavioral assays including novel object recognition, T-maze foot shock avoidance, and lever press operant conditioning task assessments. SR9009 treatment reduced amyloid-β 1-40 and 1-42 levels in the cortex, which is consistent with improved cognitive function. Furthermore, SR9009 treatment led to increased hippocampal PSD-95, cortical synaptophysin expression and the number of synapses suggesting improvement in synaptic function. We conclude that REV-ERB is a potential target for treatment of Alzheimer's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.